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Year 3 Academic Weeks > A4- Thyroid and Adrenal Disease > Flashcards

A4- Thyroid and Adrenal Disease Flashcards

1
Q
A
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2
Q

The lobes of the thyroid contain _______ , the functional units of the thyroid gland.
•Interspersed between the follicles are __ cells, which secrete calcitonin.

A

The lobes of the thyroid contain follicles, the functional units of the thyroid gland.
•Interspersed between the follicles are C cells, which secrete calcitonin.

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3
Q
  • Follicles consist of a layer of epithelium
  • Central cavities containing ____
  • Major constituent of colloid is the large _________, ________
  • Follicular cells are ____ dependent
A
  • Follicles consist of a layer of epithelium
  • Central cavities containing colloid
  • Major constituent of colloid is the large glycoprotein, thyroglobulin
  • Follicular cells are TSH dependent
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4
Q

What is the Synthesis, Storage and Secretion of thyroid hormones

A
  • Tyrosine and iodine are essential for synthesis of thyroid hormones.
  • Both are taken up by the blood
  • Tyrosine is synthesised by the body (in the thyroglobulin).
  • Iodine is a dietary essential.
  • Other endocrine glands secretes their hormones once produced, the thyroid gland stores considerable amount of the thyroid hormones in the colloid until needed.
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5
Q

Steps in biosynthesis, storage
and secretion of thyroid
hormones

A
  • Thyroglobulin produced by follicular cells and released into colloid in follicle lumen by exocytosis
  • Iodide (I-) uptake by follicular cell from the blood, oxidation (I) and transferred to colloid
  • Attachments of iodine into tyrosine residues on thyroglobulin in colloid forming di-and mono-iodotyrosine (DIT and MIT)
  • Coupling processes between the iodinated tyrosine molecules to form T4 (2DIT) and T3 (DIT + MIT)

• Secretion (upon stimulation) of T4 and T3
occurs by endocytosis, fusion with a lysosome, uncoupling of T4 and T3 and diffusion out of the follicular cell into the blood and onto peripheral tissues

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6
Q

Explain Thyroid hormone
biosynthesis

A
  • Approximately, 90% of the hormones released from the thyroid gland initially appear in the form of T4.
  • However, a majority of the T4 that is secreted from the thyroid gland is subsequently converted to T3.
  • T3 is formed from monodeiodination of T4 in the thyroid and in peripheral tissues.
  • T3 is 4 times more potent in its biologic form than T4 and is the major hormone that interacts with the target cells.
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7
Q

Clinical features of thyrotoxicosis?

A
  • Weight loss
  • Sympathetic overactivity
  • Goitre
  • Thyroid eye signs
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8
Q

Causes of thyrotoxicosis?

A
  • Graves’ disease
  • Toxic adenoma
  • Multi-nodular goitre
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9
Q

Medical and surgical management?

A

Medical
• Anti-thyroid medication (carbimazole, PTU)
• Beta-blockade
Surgical
• Sub-total thyroidectomy
• Total thyroidectomy
Radioiodine

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10
Q

Symptoms of Hypothyroidism

A
  • Fatigue
  • Lethargy
  • Weakness
  • Cold intolerance
  • Mental slowness
  • Depression
  • Dry skin
  • Constipation
  • Muscle cramps
  • Irregular menses
  • Infertility
  • Mild weight gain
  • Fluid retention
  • Hoarseness
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11
Q

Signs of Hypothyroidism

A
  • Goitre (primary hypothyroidism only)
  • Bradycardia
  • Non-pitting edema
  • Dry skin
  • Delayed relaxation
  • Hypertension
  • Slow speech
  • Slow movements
  • Voice hoarseness
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12
Q

Causes of Hypothyroidism

A
  • Autoimmune (Hashimoto’s) thyroiditis
  • Atrophic (common in elderly)
  • Iodine 131 treatment
  • pituitary
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13
Q

Antibodies in hypothyroidism

A

Anti-thyroid peroxidase (TPO) and anti-thyroglobulin (Tg )
antibodies (Hashimoto’s)

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14
Q

Hypothyroidism: Therapy

what do you use?

A

L-Thyroxine (levothyroxine; T4)

Goals of replacement
• Alleviate symptoms
• Titrate T4 intake to normalize TSH (primary
hypothyroidism) or free T4 (secondary and tertiary
hypothyroidism)

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15
Q

What is Thyroid Storm

A

Thyroid storm can be thought of as a “hyper-adrenergic” state, and many
of the symptoms of thyroid storm (hypertension, tachycardia,
palpitations, agitation, etc.) are best controlled with beta-blockade.

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16
Q

Clinical Presentation of thyroid storm

A

Anxiety, restlessness, agitation, psychosis, confusion, obtundation, coma.
• Thyrotoxic myopathy
• Cardiovascular abnormalities include
-tachycardia, AF
-CHF
• GI symptoms
-Pre-event severe weight loss
-Hyperdefecation, diarrhea
-Anorexia, N/V

17
Q

Treatment of Thyroid Storm

A

Generally supportive:
• ABC’s, intubation for comatose patient
• IV fluids: Fluid resuscitation may be required in those with
volume depletion.
• Antipyretics prn
• Treat congestive failure/pulmonary edema per protocol: Diuretics
or digoxin may be required in patients with cardiac manifestations
• Treatment of any underlying precipitating factors

18
Q

Management of thyroid storm
Thyroid based therapies

A
  1. Beta-blockade
  2. Inhibition of thyroid hormone synthesis: anti-thyroid drugs (PTU)
  3. Inhibition of thyroid hormone release (Lugol’siodine)
  4. Block peripheral conversion of T4 to T3:
    • Dexamethasone 10 mg every 6 hours or hydrocortisone 100 mg
    every 8 hours.
19
Q

What is hypothyroidsima?

A

Hypothyroidism Chronic systemic disorder characterized by progressive slowing
of all bodily functions because of thyroid hormone deficiency.

❖Primary Intrinsic failure of the thyroid gland
❖Secondary Disease of the hypothalamus and/or pituitary gland

20
Q

Myxedema Refers to?

A

severe hypothyroidism. Non-pitting, dry, waxy swelling of
the skin and SC tissue

21
Q

What is

Myxedema Coma

A

Rare complication of hypothyroidism. Usually occurs in elderly
women, during the winter as a result of stress.

22
Q

Myxoedema Coma
Clinical features

A

Altered mental status, confusion, pyschosis
Coma, 25 % seizures
Hypothermia: temp <35 oC
Bradycardia
Respiratory failure with CO2
retention
Hypoglycaemia

23
Q

Cause of Myxoedema Coma

A

Drugs: sedatives, tranquillizers
Infection
Cerebrovascular accident
Trauma

24
Q

Myxoedema Coma
Investigations

A

Hyponatraemia
Hypoglycaemia
Anaemia
Raised CK
High TSH/low T4
Cortisol
↓pO2 ↑ pCO2
Blood and urine cultures

25
Q

Myxoedema Coma
Treatment

A

Rewarm (space blanket)
Correct BP
Adequate ventilation
Broad spectrum antibiotics
Hydrocortisone 100mg IV tds
IV T3 5-20 mcg daily for 3 days
T4 25mcg daily

26
Q

Adrenal cortical layers and what do they secrete?

A
27
Q

Adrenal Cortex: Steroid Hormone Production

A
28
Q

Presentation of adrenal disease

A

•Hypofunction
•Hyperfunction:
• Cushings’ syndrome
• Conn’s syndrome
• Androgenisation
•Adrenal nodules/adenomas/masses

29
Q

Adrenal Deficicency: Causes

A

• Primary adrenal insufficiency
–chronic: undiagnosed or established and subjected to a major physiologic stress
–acute: bilateral adrenal hemorrhage, sepsis (Waterhouse-Friederichsensyndrome)

•Secondary or tertiary adrenal insufficiency
–Less common as renin-angiotensin-aldosterone axis intact

• Exogenous glucocorticoids

30
Q

When is it Adrenal deficiency/crisis

A
  • Low Na
  • High K
  • Raised urea
  • Low glucose
  • Low random cortisol
  • Synacthen test
31
Q

Causes of Cushing’s syndrome

Endogenous Causes vs Exogenous Causes

A

Endogenous Causes
• 65% = pituitary
• 25% = adrenals
• 10% = ectopic source (small cell lung ca), non-pituitary, ACTH producing tumour

Exogenous Causes
• Iatrogenic Steroids (Asthma, RA, palliative)

Higher incidence in people with: DM, HTN, Obesity and Osteoporosis

32
Q

Symptoms & Signs Cushings

A
33
Q

Differential Diagnosis: It’s not always Cushing’s
Pseudo-Cushing’s

A
  • Chronic severe anxiety and/or depression
  • Prolonged excess alcohol consumption
  • Obesity
  • Poorly controlled diabetes
  • HIV infection
34
Q

Diagnosis of Cushing’s Syndrome

A

•Obtain a careful history to exclude exogenous glucocorticoid use.
•Perform at least two first-line biochemical tests to obtain the
diagnosis:
• Urine free cortisol (UFC) (at least two measurements)
• 1-mg overnight Dexamethasone Suppression Test (ODST)
• Longer low-dose Dexamethasone Suppression Test (LDDST) (2 mg/d for 48 h)

35
Q

Dexamethasone Suppression Test

Explain results

A

Overnight Low dose = Baseline reading, Dex 1mg given at 11pm, measure cortisol at 9am
• If cortisol low (<50nmol/L) = normal
• If cortisol high (>50nmol/L) = investigate further –Cushing’s syndrome

36
Q

Ix for cushings?

A

If any positive - imaging:
•CT of adrenals
•MRI pituitary
•IPSS (inferior petrosal sinus sampling)
If ?ectopic:
•CXR
•CT =/- MRI of neck, thorax, abdomen
•Functional imaging

37
Q

Management for cushings

A

Drug therapy remains very important for normalising cortisol levels. Medical treatment
can also be used in patients who are unwilling or unfit for surgery.
• Metyrapone, ketoconazole, and mitotane can all be used to lower cortisol by directly
inhibiting synthesis and secretion in the adrenal gland.
• The treatment of choice in most patients is surgical but the metabolic consequences
increase the risk of surgery:
• increased tissue fragility
• poor wound healing
• HTN and DM

38
Q

Surgical Treatment for cushings?

A

Pituitary tumours:
• trans-sphenoidal microsurgery.
• Radiation therapy may be used as an adjunct for patients who are not cured.
• Bilateral adrenalectomy may be necessary with severe hypercortisolaemia.
Adrenocortical tumours:
• require surgical removal –can develop Nelsons Syndrome
Removal of neoplastic tissue is indicated for ectopic ACTH production
• Metastatic spread makes a surgical cure unlikely or impossible.
• Bilateral adrenalectomy may be necessary with severe hypercortisolaemia.

Year 3 Academic Weeks (40 decks)

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